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I repeated the link from someone else--Holly was that you? We are a merry gang here! so much more than any one could be

I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...http://www.thisisms.com/ftopic-7318-0.html This is my regimen threadhttp://www.ccsvibook.com Read my book published by McFarland Health topics

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if you haven't looked at the Zamboni website thread, there is good info and hope for quick world wide web access to his results.

for those of us who are searching for local practitioners and quick is not quick enough I created the reader's digest version of the sticky CCSVI that might help you get in the door. It is short and sweet but full of convincing info for that busy person you want to reach.

New Model Breaks the MS Paradigm

Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis
P Zamboni1, R Galeotti1, E Menegatti1, A M Malagoni1, G Tacconi1, S Dall’Ara1, I Bartolomei2, F Salvi2
1 Vascular Diseases Center, University of Ferrara, Ferrara, Italy
2 Department of Neurology, Bellaria Hospital, Bologna, Italy
Correspondence to:
Professor P Zamboni, Vascular Diseases Center, University of Ferrara, 44100 Ferrara, Italy; zmp@unife.itBackground: The extracranial venous outflow routes in clinically defined multiple sclerosis (CDMS) have not previously been investigated.
Methods: Sixty-five patients affected by CDMS, and 235 controls composed, respectively, of healthy subjects, healthy subjects older than CDMS patients, patients affected by other neurological diseases and older controls not affected by neurological diseases but scheduled for venography (HAV-C) blindly underwent a combined transcranial and extracranial colour-Doppler high-resolution examination (TCCS-ECD) aimed at detecting at least two of five parameters of anomalous venous outflow. According to the TCCS-ECD screening, patients and HAV-C further underwent selective venography of the azygous and jugular venous system with venous pressure measurement.
Results: CDMS and TCCS-ECD venous outflow anomalies were dramatically associated (OR 43, 95% CI 29 to 65, p<0.0001). Subsequently, venography demonstrated in CDMS, and not in controls, the presence of multiple severe extracranial stenosis, affecting the principal cerebrospinal venous segments; this provides a picture of chronic cerebrospinal venous insufficiency (CCSVI) with four different patterns of distribution of stenosis and substitute circle. Moreover, relapsing-remitting and secondary progressive courses were associated with CCSVI patterns significantly different from those of primary progressive (p<0.0001). Finally, the pressure gradient measured across the venous stenosies was slightly but significantly higher.
Conclusion: CDMS is strongly associated with CCSVI, a scenario that has not previously been described, characterised by abnormal venous haemodynamics determined by extracranial multiple venous strictures of unknown origin. The location of venous obstructions plays a key role in determining the clinical course of the disease.

...Mueller, who has recently made multiple cerebrospinal sclerosis the subject of an exhaustive treatise, goes so far as to regard the vascular involvement as secondary to the involvement of other tissues.

...venous thrombi have been described in post-infectious "encephalomyelitis" a disease which bears certain similarities to multiple sclerosis. Thrombi have been reported in cases of multiple sclerosis also, but very rarely. Their scarcity is perhaps not surprising when we consider that a thrombus in a small vessel may become so completely organized as to be unrecognizable within a week. Abnormalities in the coagulability of the blood may regularly be observed in multiple sclerosis. The sclerotic plaque may perhaps therefore be considered the mildest form of permanent damage produced by a disturbance of blood supply.

...thrombosis of a small vein leads merely to a local congestion,
which usually affects the white matter more than it does the more
vascular grey matter, and leads principally to a loss of myelin. This can
readily be demonstrated experimentally, as well as in autopsy material.
Such lesions in the acute stage present all of the histological characteristics which we associate with a condition known as ' disseminated encephalomyelitis ' or ' perivenous leucoencephalitis,' including the socalled ' inflammatory ' phenomena; the post-vaccinal, post-measles, and post-German measles forms of encephalitis are the best known examples of the type (fig. 6). In the later stages, the milder injuries resulting from vascular closure closely imitate the plaques of multiple sclerosis. I have elsewhere given evidence which suggests that these various diseases are produced by disseminated thromboses of small cerebral vessels, and that this in turn is the result of chemical changes in the blood plasma, rather than the direct effect of a specific infectious agent.

http://brain.oxfordjournals.org/cgi/pdf ... t/62/3/274Schlesinger B (1939) The Venous Drainage of the Brain. BRAIN 62(3):274
...Artificially produced perivenous extravasations of a contrastmedium
closely simulate the shape and the distribution of plaques in
advanced stages of multiple sclerosis.

guess my favourite sentence for a prize lol

Last edited by jimmylegs on Mon May 25, 2009 7:07 am, edited 2 times in total.

Thanks for all the links, Jimmy.
It infuriates me when we see how many neurologists were looking at the vascular paradigm in the early nineteen hundreds. That last Schlesinger study shows what Schelling also saw...the Dawson's Fingers pattern as related to venous back flow into the brain. This line of study was abandoned in the seventies and eighties (with the exception of Schelling), after a few clinical trials with blood thinning medications failed to produce any outstanding results....and as drug companies ran with the immune modulating therapies.

The model of the "thrombi" was what was wrong. Thrombi/clots can be de-coagulated with blood thinners. Now, with modern technology, we see the blockage is "stenosis"...a narrowing of the vein, not a clot. Stenosis won't be affected by blood thinners, but it can be addressed with endovascular techniques and blood flow can be returned. They were so close to the answer...but they couldn't see inside the veins. The neurological community kept research focused on the brain, and the vascular paradigm was dumped. 'Til now!
cheer

...Two cases of spontaneous intracerebral haemorrhage in adolescent girls suspected of having multiple sclerosis are reported. Surgical evacuation of haematomas in the left thalamus and left side of the pons, respectively, was performed with excellent recovery in both cases. Some clinical and pathological aspects of small arteriovenous malformations are discussed and the pertinent literature reviewed.

Dake has also gained international recognition for his development of stent-grafting techniques. He will be directing the Catheterization and Angiography Laboratory at Stanford University Medical Center

Dake first came to Stanford in 1990 as section chief of cardiovascular and interventional radiology and co-director of the Catheterization and Angiography Lab. During his 15 years at Stanford, his research primarily focused on endovascular device development and management of aortic pathologies. He is known for his work in the image-guided treatments for arterial disease (hardening of the arteries) and venous disease, which occurs when veins become blocked.

I didn't know where else to post this, and didn't think it deserved its own thread.

I am talking with (one of) my Neurologist who is currently running Campath trials for MS in Australia (so is pretty involved with MS).

He has read the papers by Zamboni and some others I have provided him, and although is not a "convert" as yet, he is more than willing to investigate this research. He's actually pretty sceptical of it all He was willing to run both an MRV and a CT Scan on me, but I declined the MRV, and chose the CT scan, as it was suggested by Dr Dake to be more easily reproducible and less operator sensitive.

Hopefully in the next few days he or the radiologists at his hospital will get back to me with a date and time for the test. If I show up on the CT, I think it will have a major impact on this "theory" and its acceptance in Australia. I will also see my other neurologist with my results, who is very respected in the MS world (and neurology in general, as I found dropping his name in the UK)

[quote][If I show up on the CT, I think it will have a major impact on this "theory" and its acceptance in Australia/quote]

Cure what wonderful news I am so glad for you! Is it expensive to get the MRV too? you don't think for academic purposes it might be good to just have it for comparison?

On my MRV which has the picture from dead on front, my jugs were flattened so that in the front the looked the normal thickness, but Dr Dake knew to have them digitally "turn" my picture 20 degrees and BANG! there it was the thinned area. We could see on the neck MRI too that the jugs were mere slits flattened to the back at the angle of the jaw rather than fulll round veins. SO they did slices of my neck in the regular MRI same time as MRV and that let us know that the jugs needed that rotation to see the anomaly...
marie

I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...http://www.thisisms.com/ftopic-7318-0.html This is my regimen threadhttp://www.ccsvibook.com Read my book published by McFarland Health topics

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